Wednesday, October 16, 2019

What could this rhythm be? And what is going on after it breaks?

Written by Pendell Meyers, edits by Steve Smith

A man in his 30s with no prior medical history presented with palpitations. His vitals and exam were within normal limits with the exception of his heart rate.

Here is his initial ECG:
What do you think? What is the differential?

This shows a regular narrow complex tachycardia, thus the differential is sinus tach, SVT (including AVNRT most commonly, AVRT [which is SVT in the setting of WPW with an accessory pathway] next most common, then atrial tachycardia, etc.) or atrial flutter.

It it were atrial flutter, and because it is regular at a rate of 210, the flutter would have to be conducting 1:1 to the ventricle. There are no definite atrial waves, although the negative deflections in V1 before the QRS complexes could be atrial in origin, or the entire baseline may appear to have a sawtooth pattern in lead II - it is not clear in my opinion. 1:1 atrial flutter seems unlikely because, as it would have to be 1:1 conduction, the atrial flutter rate would have to be a very slow 210 bpm (normal would be 300). The ventricular rate of roughly 210 bpm makes sinus tachycardia unlikely in a 30 year old (max sinus rate theoretically 190ish according to 220-Age rule of thumb).

Aside: if the atrial flutter rate were 300 bpm, it could not be conducted by the AV node, and the ventricular rate could only be 300 if there were an accessory pathway or a peri-AV node bypass tract that inserts into the bundle of His. In the former case, there would have to be a wide QRS (due to the preexcitation of the delta wave), but in the latter case, the QRS would be narrow.

The REVERT vagal maneuver was performed with a change in rhythm.

A repeat ECG was performed:

What do you think?

There is now a regular rhythm with wider QRS complexes than during the tachycardia above, almost imitating LBBB. There is an extremely short PR interval, such that the wide QRS takes off from the end of the P-wave. The takeoff of the QRS complex is not the most obvious delta wave, but overall this appears consistent with accessory pathway conduction, or WPW.

See these two similar cases:

A 40-something woman with no medical history presented with 2 days of chest pain

Now that we suspect the patient has an accessory pathway, the most likely rhythm responsible for his paroxysmal narrow complex regular tachycardia in the first ECG is orthodromic AVRT, in which the action potential is conducted down the AV node (causing a narrow QRS complex) and then up the bypass tract, and so on.

The patient was referred to EP for an EP study and possible ablation.

Learning Points:

You must easily be able to think through the differential of tachycardias based on the categories of narrow vs. wide QRS and regular vs. irregular rhythm:
 - Narrow & Regular
 - Narrow & Irregular
 - Wide & Regular
 - Wide & Irregular

After conversion from a regular, narrow complex tachycardia, you should always obtain a post-cardioversion ECG to look for the presence of underlying causes of the tachycardia, most commonly WPW syndrome.

WPW can distort the QRS complex and mimic bundle branch blocks or other conduction abnormalities, without showing the classic delta wave into an otherwise normal, narrow QRS complex. The risk in this case is that WPW is missed due to the confusing QRS morphology.

Some bypass tracts are "concealed" meaning they do not conduct during normal sinus rhythm and thus leave no evidence on the resting sinus ECG.

MY Comment by KEN GRAUER, MD (10/16/2019):
Excellent case for discussion presented by Drs. Meyers & Smith! I would add the following comments regarding selected concepts of arrhythmia diagnosis and management:

Use a Systematic Approach: There are KEY parameters to assess when confronted with any cardiac arrhythmia. These 6 parameters are:
  • #1) Is the patient hemodynamically stable? This clearly is the 1st thing to assess — since if the patient is not hemodynamically stable because of the arrhythmia — then immediate cardioversion is indicated regardless of whether one is dealing with VT or an SVT.
The Next 5 Parameters constitute what needs to be assessed regarding the arrhythmia itself. I find it easiest to remember these parameters by the saying, Watch your Ps, Qs and the 3 Rs”:
  • Are there P waves? And, if there aren’t clearly identifiable P waves — Is there evidence of atrial activity, such as “fib” or “flutter” waves?
  • Is the QRS complex wide or narrow?
  • What is the Rate?
  • Is the rhythm Regular?
  • If P waves are present — Are they Related” to neighboring QRS complexes?
  • CLICK HERE if interested in more on using the “Ps, Qs & 3Rs” Approach.

Figure-1: The 2 ECGs in this case (See text).

Assessing the 6 Parameters in This Case:
For clarity — I’ve put the 2 tracings in this case together in Figure-1. Although there is some angulation of these tracings — measurements are intact.
  • Regarding the 6 Parameters: The patient in this case was symptomatic with “palpitations” — but this man in his 30s was hemodynamically stable with normal vital signs other than a fast heart rate.
  • Normal sinus P waves (ie, upright P waves in lead II) are not seen. There may be 1:1 retrograde activity (RED arrows in ECG #1) — but if these sharper-than-expected deflections do reflect retrograde atrial activity — the RP’ interval would be relatively long (occurring well within the ST segment). RP’ intervals occurring well within the ST segment are too long to be consistent with AVNRT — but could be consistent with anterograde AVRT (since it takes more time for retrograde conduction over an accessory pathway that lies further away, because it is outside of the AV node).
  • The QRS complex is narrow (ie, clearly not more than half a large box in duration in any of the 12 leads in ECG #1).
  • The 3 Rs: The ventricular rhythm is extremely Regular — the Rate is ~210/minute — and although no sinus P waves are present, P waves could be Related” to neighboring QRS complexes by 1:1 retrograde = VA conduction.
CONCLUSION: The patient is hemodynamically stable. The rhythm in ECG #1 is a regular SVT (SupraVentricular Tachycardia) at ~210/minute without clear sign of sinus P waves. As mentioned, there may be 1:1 retrograde atrial conduction — but it is difficult to be certain about this from ECG #1. As per Dr. Meyers — the principal differential diagnosis of a regular SVT without clear sign of sinus P waves includes: i) Sinus Tachycardiaii) Reentry SVT (either AVNRT if the reentry circuit is contained within the normal AV nodal pathway — or AVRT if an accessory pathway is involved)iii) Atrial Tachycardiaor iv) Atrial Flutter.

NOTE: It is worth spending a moment on how we determined the heart Rate — since accurate estimation of rate can sometimes be extremely helpful in determining which of the above diagnostic considerations is the most likely cause of a regular SVT rhythm.
  • When the rhythm is fast and regular — the Every-Other-Beat Method allows rapid and accurate rate estimation. Find a QRS complex that begins on a heavy line. We chose the 2nd beat in lead I (See the 1st vertical RED line under this beat in lead I of ECG #1).
  • The amount of time (ie, the R-R interval) that it takes to record 2 beats (BLUE numbers in lead II) is just under 3 large boxes (RED numbers in lead I). Therefore — HALF the rate is a little faster than 300/3 ~105/minute.
  • The actual rate for the rhythm in ECG #1 is therefore ~105 X 2 = 210/minute.
  • CLICK HERE if interested in brief video review of this Every-Other-Beat Method.

How Heart Rate Helps in SVT Diagnosis:
  • Although the formula for estimating the maximal rate of sinus tachycardia for stress testing (ie, during exercise) is ~ 220 minus Age — in my experience, it is highly unlikely (though not impossible) for sinus tachycardia in a horizontal" adult patient (ie, in a patient you are examining, who has not just been running) to exceed 170/minute. This statement does not hold true for children — as sinus tachycardias over 200/minute are not that uncommon in the pediatric age group. But the rate of 210/minute for the patient in this case essentially rules out sinus tachycardia.
  • The most common ventricular response to untreated AFlutter is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range 250-350/minute— and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. Therefore (as per Dr. Meyers) — the SVT in this case at a rate of ~210/minute is highly unlikely to be AFlutter in this previously healthy man in his 30s, since this would entail a flutter rate of 210 X 2 = 420/minute, which is much faster the atrial rate for flutter. NOTE: This rate range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial (and therefore ventricular) rate for flutter.
  • Finally — Although listed in the above differential diagnosis — ATach is far less common as a cause for a strictly regular SVT as seen in ECG #1 compared to AVNRT or AVRT, especially in a previously healthy younger adult.
  • THEREFORE  By the process of elimination, the most likely cause of the regular SVT at ~210/minute in ECG #1 is a reentry tachycardia. And, if the RED arrows we’ve drawn in ECG #1 do in fact represent retrograde atrial activity with a long RP' interval — then it’s likely this patient has WPW (CLICK HERE for review of the common arrhythmias encountered with WPW).
  • PEARL: From the above, it can be seen that if the regular SVT is at a rate close to 150/minute (ie, 140-160/minute) — that any of the 4 diagnostic entities listed above could be present (sinus tach/AVNRT-AVRT/ATach/AFlutter). It is when the rate of a regular SVT without clear sign of sinus P waves is substantially faster than this — that a reentry SVT (AVNRT/AVRT) becomes by far the most likely diagnosis!

FOLLOW-UP: As per Dr. Meyers — ECG #2 was obtained after the vagal maneuver. I’ve drawn BLUE arrows to highlight those leads in which delta waves are seen — which confirms the diagnosis of WPW.

Should This Patient be Ablated?
The patient in this case was a previously healthy man in his 30s, who presented with “palpitations”. There is no mention of prior episodes of SVT. There is no mention of drug therapy — only that the REVERT vagal maneuver was performed and was successful. Is EP referral for ablation the optimal course of treatment for this patient? In my opinion — the answer is not a yes — but rather, Idepends” ...
  • Clearly the approach to treatment of numerous cardiac arrhythmias has changed in recent years, with ever increasing expertise in the exciting field of cardiac electrophysiology. But even in the best of centers with the most experienced of EP cardiologists — ablation IS a procedure, and there IS potential for adverse effect.
  • If I was a previously healthy 30-year old man with a 1st episode of a hemodynamically tolerated SVT that was easily resolved by simple vagal maneuver (without even need for antiarrhythmic medication) — I would not opt for an invasive procedure with potential for significant side effects as my 1st intervention (despite VERY high likelihood for “cure” of this arrhythmia with very low chance of adverse effect). “Low risk” is not the same as “NO risk” — and if I was the patient, I'd prefer to start with a far less invasive intervention.
  • That said — there is notYes-or-No answer to this question. I’m simply suggesting that rather than automatically referring this patient to EP cardiology for ablation of his accessory pathway at this point — that an appropriate alternative course might be diligent follow-up while teaching this patient vagal maneuvers that he can perform at home on his own (ie, Valsalva), perhaps with a prn antiarrhythmic “cocktail” (ie, a single dose of beta-blocker or diltiazem or verapamil) that can be tried if this hemodynamically stable SVT recurs. Recurrence of this SVT might be infrequent (if it recurs at all), and it might again be easily managed — possibly even without need for daily antiarrhythmic therapy.
  • NOTE: ED referral of this patient for follow-up care IS of course indicated! — but such follow-up need not necessarily be to an EP cardiologist (or even necessarily to a cardiologist). Of course — IF repeated episodes occurred despite appropriate antiarrhythmic medication — that would be a different story (in which case, referral to your friendly EP cardiologist becomes the optimal management approach). Along the way to guiding optimal decision-making for this case — informed patient consent and patient preference are critical.
  • CLICK HERE for more on “My Take” on How to Advise the Patient with WPW.

Our THANKS to Drs. Meyers and Smith for presenting this case!


  1. Thanks again for another great case!

    Q. Can LGL Syndrom be an option when I interpret short PR interval?
    Q. Does it exist?

    Thanks in advance!

    1. @ Anonymous. THANKS for the kind words. LGL ( = Lown-Ganong-Levine) — is a syndrome that in the past referred to the finding of a short PR interval (<0.12 second, in adults), but a normal (narrow) QRS complex and no delta waves. The thought was that this short PR interval indicated the presence of an AP (accessory pathway) passing from atria-to-ventricles, but without passage through ventricular myocardial muscle that results in slowed conduction with resultant delta waves. With realization that OTHER phenomena not due to existence of an AP may also cause shortening of the PR interval (ie, accelerated conduction through the AV node; an anatomically smaller-than-usual size of the AV node) — application of the term, LGL should now be reserved for cases when there is: i) a short PR interval; ii) an otherwise normal QRS complex (no delta waves!); — AND — iii) clinical documentation of cardiac arrhythmia that may be the result of an AP. In this particular case — since the QRS complex in ECG #2 is wide AND has delta waves — there is evidence of WPW (but this is clearly not LGL) — :)

  2. In the initial discussion in states that SVT could be "AVRT [which is SVT in the setting of WPW with an accessory pathway]". I think this isn't quite accurate as a description. WPW suggests that the accessory pathway can conduct top to bottom causing a delta wave. Narrow QRS AVRT doesn't necessarily require an accessory pathway that can conduct top to bottom. Since the QRS is narrow complex on EKG 1 and you can have an accessory pathway that conducts ONLY bottom to top, the ddx would include AVRT but this wouldn't have to be in the setting of WPW syndrome. While AVRT and WPW often live together, they don't have to. Is this right?

    1. @ Anonymous — You are correct! You can have a narrow reentry SVT rhythm that does NOT involve an AP (accessory pathway) — in which case the rhythm is termed, “AVNRT”. I indicate this in My Comment above (in the paragraph beginning, “Conclusion”). I suspect your wrote your question before I had a chance to include My Comment (Please realize that I have to wait until AFTER each blog post is published before I get to see the tracings … therefore My Comment is usually delayed by 12-48 hours — :)

  3. Great case, sir. Can you update the EPS result? Where is the location of the AP? Thank you :)

    1. @ Anonymous — Thanks for your comment. I will ask Drs. Meyers and Smith if they have any information on the official EP result for this patient. In the meantime — I’ll share my synthesis of the best references I’ve seen for predicting the likely localization of the AP (Accessory Pathway) — References that I used, and details of the synthesized Algorithm I developed can be found HERE — — For this case, I’ll use the post-conversion tracing that shows WPW ( = ECG #2 in my Figure-1 above, in which BLUE arrows highlight some of the delta waves that we can see). The 1st Step in my method is to determine the area of Transition (where the R wave becomes greater than the S wave in the chest leads). This looks to be between leads V3-to-V4 — therefore begin with STEP B-4 in my algorithm. While admittedly difficult to tell (because the limits of the delta wave in lead II are not clearly demarcated) — I took the delta wave in lead II to be less than 1.0mV (10 mm) — which suggests the AP is in the RV Free Wall. Next according to the algorithm — GO to STEP B-5 — in which we are to measure the delta wave frontal axis — which is positive, because the delta wave is positive in both leads I and aVF. This suggests the AP is in the Anterolateral RV Free Wall. NOTE — This algorithm is NOT perfect (I believe NO algorithm is perfect for localizing the AP on ECG prior to EP study) — but I’ve liked this algorithm at the above link, because it is EASY to use (it takes no more than 1-2 minutes) and as accurate as anything I’ve encountered — :)

    2. Sorry, I don't have access to the EP study results.

    3. I think of it simply: if it looks like LBBB (like this one), then there is a right sided AP (depolarization coming right to left, as in LBBB). If it looks like RBBB (like this one), then there is a left sided AP (depolarization coming left to right, as in RBBB).

  4. There are ST depression in inferior and V3-V4 leads, but ST elevation in V2-3 and aVR.These depression Coud be pharmacological effect of digitalis?

    1. The pattern of ST segment deviation that we see here (ie, ST depression in no less than 8 leads — with ST elevation in aVR & V1) is suggestive of subendocardial ischemia and NOT digitalis effect or digitalis toxicity. That said — given the heart rate in ECG #1 ( ~210/minute) — the chances are great that the principal cause of these ST-T wave changes is tachycardia — which can be determined by repeating the ECG after conversion to sinus rhythm (in which case most, if not all of the ST depression and elevation will probably resolve). Alas, in this case — ECG #2 (in my Figure-1 above) shows that there is preexcitation (WPW) in the post-conversion tracing — so we are not really able to assess serial ST-T wave changes. In any event — these ST-T wave changes are unlikely to be the result of digitalis effect or toxicity — :)


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